Andrographolide enhances redox status of liver cells by regulating microRNA expression.
Antioxidants
/ pharmacology
Diterpenes
/ pharmacology
Gene Expression Regulation
/ drug effects
Glutathione Peroxidase
/ genetics
Heme Oxygenase-1
/ genetics
Hep G2 Cells
Hepatocyte Nuclear Factor 4
/ genetics
Hepatocytes
/ drug effects
Humans
Liver
/ drug effects
MicroRNAs
/ genetics
NF-E2-Related Factor 2
/ genetics
Oxidation-Reduction
/ drug effects
Oxidative Stress
/ drug effects
Receptor, Adenosine A2A
/ genetics
Signal Transduction
/ drug effects
Thioredoxins
/ genetics
Tumor Suppressor Protein p53
/ genetics
Liver/hepatocytes
Oxidative stress
Transcription/transcription factors
Journal
Free radical biology & medicine
ISSN: 1873-4596
Titre abrégé: Free Radic Biol Med
Pays: United States
ID NLM: 8709159
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
19
09
2018
revised:
03
11
2018
accepted:
04
11
2018
pubmed:
12
11
2018
medline:
18
12
2019
entrez:
12
11
2018
Statut:
ppublish
Résumé
Andrographis paniculata Nees and its principal compound andrographolide are well known for exerting beneficial effects by modulating signaling pathways in different biological systems. Our earlier studies have demonstrated the ability of andrographolide as well as andrographolide enriched extracts to activate Nrf2/HO-1 pathway through adenosine A
Identifiants
pubmed: 30414976
pii: S0891-5849(18)31669-1
doi: 10.1016/j.freeradbiomed.2018.11.004
pii:
doi:
Substances chimiques
Antioxidants
0
Diterpenes
0
HNF4A protein, human
0
Hepatocyte Nuclear Factor 4
0
MIRN17 microRNA, human
0
MIRN224 microRNA, human
0
MIRN377 microRNA, human
0
MIRN433 microRNA, human
0
MicroRNAs
0
NF-E2-Related Factor 2
0
NFE2L2 protein, human
0
Receptor, Adenosine A2A
0
TP53 protein, human
0
Tumor Suppressor Protein p53
0
andrographolide
410105JHGR
Thioredoxins
52500-60-4
Glutathione Peroxidase
EC 1.11.1.9
HMOX1 protein, human
EC 1.14.14.18
Heme Oxygenase-1
EC 1.14.14.18
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
397-407Informations de copyright
Copyright © 2018 Elsevier Inc. All rights reserved.